BackgroundArsenic is an environmentally harmful substance that causes hepatic insulin resistance and liver damage, increasing the risk of ty
BackgroundArsenic is an environmentally harmful substance that causes hepatic insulin resistance and liver damage, increasing the risk of type 2 diabetes mellitus. ObjectiveTo explore whether the insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) is involved in insulin resistance in HepG2 cells after arsenic exposure through the peroxisome-proliferator-activated receptor γ (PPAR-γ) / glucose transporter 4 (GLUT4) pathway. MethodsCell viability was determined using cell counting kit 8 (CCK8) and an appropriate NaAsO2 infection dose was determined. A cellular arsenic exposure model of HepG2 cells was established by four concentrations of NaAsO2 solution for 24 h (the experiment was divided into four groups: 0, 2, 4, and 8 μmol·L−1); HepG2 cells were firstly treated with pcDNA3.1-IGF2BP2 and pcDNA3.1-NC respectively for 6 h, then with 8 μmol·L−1 NaAsO2 for 24 h to establish a IGF2BP2 overexpression cell model (the experiment was divided into 4 groups: control, NaAsO2, NaAsO2+pcDNA3.1-IGF2BP2, and NaAsO2+pcDNA3.1-NC); finally the cells were subject to 100 nmol·L−1 insulin stimulation for 30 min. Glycogen and glucose in HepG2 cells were determined by glycogen and glucose assay kits; mRNA expression levels of IGF2BP2 were measured by quantitative real-time PCR; protein expression levels of IGF2BP2, PPAR-γ, and GLUT4 in HepG2 were detected by Western blot (WB); and the binding of IGF2BP2 to PPAR-γ and PPAR-γ to GLUT4 was verified by co-immunoprecipitation (CO-IP) experiment. ResultsThe results of CCK8 experiment showed a dose-effect relationship between NaAsO2 concentration and cell viability. When the concentration of NaAsO2 was ≥4 μmol·L−1 , the cell viabilities were lower than that of the control group (P
